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A group of Australian scientists have been able to cure HIV in mice by boosting their immune systems.

Doctor Marc Pellegrini from Melbourne's Walter and Eliza Hall Institute found a hormone known as Interleukin 7 stimulates the body's response to an infection, causing it to clear the virus.

This process is called immune exhaustion.

"We found that Interleukin 7 boosted the immune response in a pretty profound fashion, such that animals were able to gradually clear the virus without too much collateral tissue damage," Dr Pellegrini said.

"The findings could lead to a cure for chronic viral infections like HIV, hepatitis B and C, and bacterial infections such as tuberculosis."

This article about the mice study sheds a little more light on how IL-7 enabled the mice's immune system to eradicate HIV (or an HIV-like virus as this article states). HIV causes a gene called SOCS-3 to become overactivated, and this gene suppresses the immune system. IL-7 switches off SOCS-3.

A study on mice with an HIV-like infection found that boosting their immune systems cured them of the disease.Scientists at the Walter and Eliza Hall Institute in Australia said their findings could help develop drugs to help people rid their bodies of infections such as HIV, hepatitis B and C and tuberculosis.In mice infected with the HIV-like illness, they looked at the role of IL-7, a naturally-occurring immune hormone.In the face of an infection such as HIV, a gene called SOCS-3 halts the immune system.However, it was found that boosting the levels of IL-7 switched off the gene and allowed the mice to gradually fight the illness.According to the Daily Mail, Dr Marc Pellegrini, of the Walter and Eliza Hall Institute, said: “Viruses such as HIV and hepatitis B and C overwhelm the immune system, leading to establishment of chronic infections that are lifelong and incurable.“Despite tremendous efforts, long-lived immune responses for some of these viruses are ineffective, because the body is so overrun by virus that the immune system just give up trying to battle the infection. “Some people have coined the phrase ‘immune exhaustion’ to explain the phenomenon. “Our approach is to discover some of the mechanisms that cause this immune exhaustion, and manipulate host genes to see if we can boost the natural immune response in order to beat infection.”The study was published in the journal Cell today.

Scientists have discovered a treatment that could eliminate the Aids-causing virus from the system and allow the body to cure itself.

It has been known that HIV’s persistent attack on the body overwhelms the defence or the immune system, eventually wearing down the white blood cells.

White blood cells or T-cells are primarily responsible for fighting off foreign organisms that enter the body.

Like an army

Just like in an army that is constantly at war, the solders, in this case the white blood cells, can become exhausted and give up, leaving the body defenceless and open to opportunistic infections.

In such a case, the military commander, knowing that he is fighting a losing war, may decide to surrender to avoid more damage. The body has a similar mechanism.

Scientists have also discovered that overproduction and excitement of white blood cells can damage some other body tissues and sometimes lead to leukaemia, a type of blood cancer.

The overproduction of white blood cells or an overworked immune system in people with HIV and other chronic infections has been associated with the possible development of cancers and heart disease.

Now Australian scientists at the Walter and Eliza Hall Institute have manipulated this mechanism to ensure the production and activation of white blood cells does not stop but goes on until HIV and other viruses have been eliminated from the body.

In a press statement released by the institute on Friday, the researchers said they manipulated the gene SOCS-3, which orders the “surrender” of white blood cells, with a hormone called IL-7.

When the researchers increased levels of the hormone IL-7, the gene SOCS-3 “switched off” and the trial mice were able to gradually eliminate the HIV from their bodies, says the main study published in the February 4 issue of the journal Cell.

Overwhelming infection

“In an overwhelming infection like HIV, SOCS-3 becomes highly activated and suppresses the immune response, probably as a natural precaution to prevent ‘out of control’ responses that cause collateral damage to body tissue,” Dr Marc Pellegrini, the lead researcher, said in the statement.

“In the case of these overwhelming infections, the immune system effectively slams on the brakes too early, and the infection persists.”

Switching off the SOCS-3 gene made sure the white cells remained active and helped the lab mice completely eliminate the infection.

The switch off and immune boost were timed to be long and strong enough to eliminate the virus without causing damage to other body tissues.

Dr Pellegrini said the research had provided excellent ideas for new treatments that could target and boost immune cells to fight disease, rather than targeting the disease itself.

“The findings could help to develop drugs that target some of these host molecules, such as SOCS-3, and turn them off for very short, defined periods of time to reinvigorate the T-cells, allowing them to regroup to fight infection,” he said.

The researchers say their work raises a real possibility for a possible cure not only for HIV but for other long-term infections, including hepatitis B and C and tuberculosis.

Despite tremendous efforts, long-lived immune responses for some of these viruses are ineffective because the body is so overrun by the virus that the immune system gives up trying to battle the infection.

Anti-retroviral treatment

An estimated 1.5 million Kenyans are infected with HIV, of which about a third are on antiretroviral treatment. Antiretrovirals work by suppressing the replication of the virus in the body and are a life-long treatment.

Like most other medicines for chronic diseases, they sometimes cause serious side effects, and a patient is advised to be in constant communication with a qualified clinician.

It is a known fact that these mouseez got their AIDS in an immaculate manner. For all we know they only practiced oral sex prior to their infection.

Logged

"I have tried hard--but life is difficult, and I am a very useless person. I can hardly be said to have an independent existence. I was just a screw or a cog in the great machine I called life, and when I dropped out of it I found I was of no use anywhere else."

Some of these other IL-7 trials seem to have different endpoints (such as how it affects CD4 count) that don't involve looking at levels of SOCS-3. Would be nice to do a study on humans looking specifically for this.

IL-7 and its effect on reservoirs has been observed for several years now. Research does seem to move at a glacial pace sometimes.

I'm trying to understand some of the conflicting findings re: IL-7. This article from hiv-reservoir.net in December contradicts previous findings that IL-7 strongly activating latent HIV in humans.

But the recent finding in mice studies is that a key gene, SOCS-3, dampens the immune response in response to being over activated by HIV. IL-7 shuts off SOCS-3 inside t-cells, enabling the mice's immune system to purge HIV. So, I'm not sure if it's relevant whether IL-7 activates latent HIV so that HAART can attack newly awakened HIV. The articles above re: mice suggest IL-7 has a totally different MOA. By boosting memory cells, and vastly improving their functionality, they are able to naturally fight HIV, including the HIV reservoirs.

A recently published study shows that HIV viruses detected during episodic blips following interleukin-7 administration are similar to the viruses present before and after IL-7 therapy. This is bad news for eradication trials planning to use IL-7 to ‘purge’ HIV reservoirs.

Since the work of Roger Pomerantz group in 2005 (1), IL-7 is considered as a cytokine able to reactivate HIV in silent HIV reservoirs. Trials are ongoing or planned, which combine potent anti-retroviral combinations and IL-7 to ‘flush out’ the HIV reservoir (2).

An informative study published in AIDS (3) shows that the low level viremia induced by IL-7 likely reflects predominantly transient induction or release of virus from a preexisting pool rather than activation of silent quasispecies.

The study participants were HIV-1-infected adults who had plasma HIV-RNA levels less than 50 copies/ml and CD4 T-cell counts at least 100 cells/ml at screening and had received HAART for a minimum of 12 months. Participants received a single dose of subcutaneous recombinant human IL-7 on day 0. Plasma and PBMCs (5 x 106) samples were obtained at baseline (day 0 of recombinant human IL-7 therapy), during the episode of viral blips (day 4), and at a time when levels of plasma HIV-RNA had returned to less than 50 copies/ml(day 28).

Transient ‘blips’ in plasma viremia were detected during the days of observed peak T-cell proliferation (day 4) and increased T-cell counts (day 14) in seven of 15 recombinant human IL-7 recipients with HIV-RNA less than 50 copies/ml at study entry. The magnitude of the blips was low (median: 79 copies/ml, range: 56–154 copies/ml). Levels of proviral DNA remained stable during the 28-day sampling period. Baseline level of provirus did not appear to predict the likelihood of blipping during IL-7 therapy.No increase in genetic diversity was observed. Overall, the plasma virus detected on day 4 was indistinguishable from the viral quasispecies present at day 0 and 28 within an individual patient. The episodic blips did not have any substantial impact on the distribution pattern of PBMCs proviral DNA. Instead, the diverse provirus population present at baseline persisted throughout the sampling period.

In conclusion, the viruses detected at the times of episodic HIV viremia were derived from the same sources giving rise to viruses in plasma before and after recombinant human IL-7 therapy, and it is likely that recombinant human IL-7 is inducing a transient viral burst primarily by amplifying virus present before IL-7 therapy, rather than inducing production from previously silent reservoirs.

It's good to have a general idea, but humans are different than animals.For example, the widely used artificial sweetener aspartame causes cancer in female and male mice, and male rats, but not in female rats and in humans!

IL-7 could trigger a leukemia in humans, so it will be a tricky approach.

It's good to have a general idea, but humans are different than animals.For example, the widely used artificial sweetener aspartame causes cancer in female and male mice, and male rats, but not in female rats and in humans!

IL-7 could trigger a leukemia in humans, so it will be a tricky approach.

Those mice have a humanized immune system so that it is more similar to a human being's system.

I can definitely see all the wacko family first political parties out protesting over the curing of HIV in mice. Now without HIV what's going to stop all the mice going out and having rampant, unprotected sex? And heaven forbid, all the gay mice will be out fornicating and destroying mouse family values. Next they'll want gay mouse marriage rights.

Although this does solve the issue of having to carry around mouse frangers. How are they expected to carry around their little love sheaths when they don't have pockets.